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Cerebral toxoplasmosis with multiple hemorrhage lesions in an HIV infected patient: A case report and literature review
Institution:1. Laboratório de Doenças Transmissíveis, Departamento de Parasitologia, Centro de Pesquisas Aggeu Magalhães, Av. Prof. Moraes Rego, s/n, Recife, PE, 50670 420, Brazil;2. Department of Neurology, Faculdade de Ciências Médicas, Universidade de PernammbucoRua Arnóbio Marques, 310 – Santo Amaro, Recife/PE CEP: 50100-130, Brazil;3. Laboratório de Imunopatologia Keizo Asami, Av. Prof. Moraes Rego, 1235–Cidade Universitária, Recife, PE, CEP: 50670-901, Brazil;1. Department of Hematology and Oncology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-Ku, Tokyo, 113-8655, Japan;2. Department of Cell Therapy and Transplantation Medicine, The University of Tokyo Hospital, 7-3-1 Hongo, Bunkyo-Ku, Tokyo, 113-8655, Japan;3. Department of Radiology, The University of Tokyo Hospital, 7-3-1 Hongo, Bunkyo-Ku, Tokyo, 113-8655, Japan;4. Department of Pathology, The University of Tokyo Hospital, 7-3-1 Hongo, Bunkyo-Ku, Tokyo, 113-8655, Japan
Abstract:A 47-year-old man was admitted to a hospital for disturbance of consciousness. He was diagnosed with multiple hemorrhagic brain abscesses in bilateral hemispheres with human immunodeficiency virus (HIV) infection, and was transferred to our hospital for further examination and treatment. On admission, although he could respond to pain stimuli, he could not talk or communicate. His laboratory data on admission revealed CD4-positive T cell count of 67 cells/μL, and HIV1-RNA viral load of 5.6 × 105 copies/mL. Both the serum IgG Toxoplasma gondii antibody and the cerebrospinal fluid polymerase chain reaction for Toxoplasma gondii DNA were positive. He was diagnosed with cerebral toxoplasmosis and HIV infection. His level of consciousness worsened, and the number of hemorrhagic lesions had increased in both hemispheres and the left thalamus on the computed tomography scan following two weeks of antitoxoplasma therapy. These newly discovered hemorrhagic lesions revealed in the CT had been found as the high intensity signal regions of initial fluid-attenuated inversion recovery magnetic resonance imaging. After five weeks of treatment, the hemorrhagic lesions gradually improved along with the patient's consciousness. Antiretroviral therapy was initiated six weeks following antitoxoplama therapy with reassurance that immune reconstitution inflammatory syndrome did not occur. After approximately four months of antitoxoplasma therapy, the patient was discharged into a group home with residual left hemiparesis on maintenance antitoxoplasma and antiretroviral therapy. Clinicians should recognize the delay of clinical and radiological improvement for hemorrhagic cerebral toxoplasmosis and patiently continue the antitoxoplasma therapy.
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